Abstract

Research on psoriasis pathogenesis has largely increased knowledge on skin biology in general. In the past 15 years, breakthroughs in the understanding of the pathogenesis of psoriasis have been translated into targeted and highly effective therapies providing fundamental insights into the pathogenesis of chronic inflammatory diseases with a dominant IL-23/Th17 axis. This review discusses the mechanisms involved in the initiation and development of the disease, as well as the therapeutic options that have arisen from the dissection of the inflammatory psoriatic pathways. Our discussion begins by addressing the inflammatory pathways and key cell types initiating and perpetuating psoriatic inflammation. Next, we describe the role of genetics, associated epigenetic mechanisms, and the interaction of the skin flora in the pathophysiology of psoriasis. Finally, we include a comprehensive review of well-established widely available therapies and novel targeted drugs.

Highlights

  • 15 years, breakthroughs thePublished: understanding the pathogenesis of psoriasis have been translated into targeted and highly effective therapies providing fundamental insights into

  • The interaction between ACT1 and the IL-17 receptor complex leads to the activation of a series of intracellular kinases including: extracellular signal-regulated kinase (ERK), p38 MAPK, TGF-beta-activated Kinase 1 (TAK1), I-kappa B kinase (IKK), and glycogen synthase kinase 3 beta (GSK-3 beta)

  • A systematic review concluded that the evidence is insufficient to make general therapeutic recommendations for tonsillectomy, except for selected patients with recalcitrant psoriasis, which is clearly associated to tonsillitis [162]

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Summary

Definition and Epidemiology

Psoriasis is a chronic inflammatory skin disease with a strong genetic predisposition and. 1. Definition and Epidemiology autoimmune pathogenic traits. The worldwide prevalence is about 2%, but varies according to Psoriasis is aa lower chronic inflammatory skin disease withAfrican a strong genetic predisposition regions [1]. It shows prevalence in Asian and some populations, and up to and. 2%, but varies according to Caucasian and Scandinavian populations [2,3,4,5]. It shows a lower prevalence in Asian and some African populations, and up to 11% in

Clinical
Clinical manifestations
Psoriasis
Inverse Psoriasis
Guttate
Pustular psoriasis
Comorbidities
Onycholysis
Pathogenesis
Pathophysiology in Variants
Autoimmunity in Psoriasis
Genetics
Antigen Presentation
Epigenetics
Microbiome
Method
Therapy
Small-Molecule Therapies
Biologics
Biosimilars in Psoriasis
Drugs in the Research Pipeline
Findings
Outlook
Full Text
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